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1. Changes in some enzymatic activities and content of -SH group of the skin of mice during carcinogenesis induced by methylcholanthrene were investigated.

(一)对表皮LDH、ATP酶、組織蛋白酶的某些性貭作了初步研究。(二)在甲基胆蒽誘发皮肤癌过程中,观察到:(1)組織提取液的蛋白貭含量有所增高;(2)GDH、GOT、谷氨酰胺酶的活性显著降低;(3)LDH的活性显著增高;(4)組織蛋白酶与二肽酶活性在增生期有所增高;在乳头瘤及皮肤癌則略有降低;(5)ATP酶活性无显著变化;(6)在增生期蛋白—SH基增多,非蛋白—SH基減少;乳头瘤与皮肤癌的蛋白—SH基接近正常,非蛋白—SH基增多。(三)在皮肤引癌早期,如滴甲基胆蒽一次后2斗小时,GDH活性即显著下降,而LDH活性仍接近正常。(四)滴非致癌物,蒽对表皮GDH及LDH活性无显著影响。(五)結合形态学的观察,对上述酶活性及—SH基变化在皮肤癌变中的可能意义,作了簡短討論。

Mice inoculated with Ehrlich ascites carcinoma cells were intraperitoneally injected on the 8th day with actinomycin K. The animals were killed 6 hours after injection.

小白鼠接种Ehrlich腹水癌細胞后第8天,腹腔注射生理盐水(对照組)或放线菌素K,6小时后解剖,研究放綫菌素K对癌細胞核酸等含量的影响。当放綫菌素K的剂量为50微克/公斤体重(治疗剂量)时,6小时后每毫克干重癌細胞中酸溶磷、脂溶磷、RNA和DNA的含量都沒有变化。增高剂量为400微克/公斤时,每毫克干重癌細胞中酸溶磷、无机磷、脂溶磷、核蛋白氮以及DNA的含量仍沒有明显改变,但RNA含量則降低。以細胞为单位作比較,結果也一致。若于接种后第3天开始給药,剂量为50微克/公斤/天,共5天,停药后6小时解剖。每单位細胞的干重稍有減低,但經t测驗比較,相差不显著。每单位癌細胞中酸溶磷、脂溶磷和DNA沒有明显影响,RNA則下降更甚而核蛋白氮也开始減少。若以干重为单位比較,RNA仍有很大降低,核蛋白氮相差不明显而DNA反有显著升高。于一次注射药物后2小时,皮下注射Na_2HP~(32)O_41微居里/克体重,再隔4小时后解剖,比較对照組和給药組癌細胞中酸溶磷、无机磷和RNA的比放射強度(脉冲数/分钟/微克磷)。发現給药組酸溶磷和无机磷的比放射強度,不論剂量为50或400微克/公斤,都不变。RNA的...

小白鼠接种Ehrlich腹水癌細胞后第8天,腹腔注射生理盐水(对照組)或放线菌素K,6小时后解剖,研究放綫菌素K对癌細胞核酸等含量的影响。当放綫菌素K的剂量为50微克/公斤体重(治疗剂量)时,6小时后每毫克干重癌細胞中酸溶磷、脂溶磷、RNA和DNA的含量都沒有变化。增高剂量为400微克/公斤时,每毫克干重癌細胞中酸溶磷、无机磷、脂溶磷、核蛋白氮以及DNA的含量仍沒有明显改变,但RNA含量則降低。以細胞为单位作比較,結果也一致。若于接种后第3天开始給药,剂量为50微克/公斤/天,共5天,停药后6小时解剖。每单位細胞的干重稍有減低,但經t测驗比較,相差不显著。每单位癌細胞中酸溶磷、脂溶磷和DNA沒有明显影响,RNA則下降更甚而核蛋白氮也开始減少。若以干重为单位比較,RNA仍有很大降低,核蛋白氮相差不明显而DNA反有显著升高。于一次注射药物后2小时,皮下注射Na_2HP~(32)O_41微居里/克体重,再隔4小时后解剖,比較对照組和給药組癌細胞中酸溶磷、无机磷和RNA的比放射強度(脉冲数/分钟/微克磷)。发現給药組酸溶磷和无机磷的比放射強度,不論剂量为50或400微克/公斤,都不变。RNA的比放射強度則下降:50微克/公斤組降低40%,400微克/公斤組降低52%。

In the 3'-MeDAB induced liver tumour, it was found that the activities of glucoses-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase and dipeptidases were higher than those in the normal liver, while the activities of glutamic dehydrogenase, glutaminase(phosphate-activated), ornithine carbamyl transferase, tryptophan pyrrolase, threonine dehydrase and tyrosine transaminase were lower or even absent.Changes in most enzyme activities were observed in the precancerous stage and the pattern of these changes...

In the 3'-MeDAB induced liver tumour, it was found that the activities of glucoses-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase and dipeptidases were higher than those in the normal liver, while the activities of glutamic dehydrogenase, glutaminase(phosphate-activated), ornithine carbamyl transferase, tryptophan pyrrolase, threonine dehydrase and tyrosine transaminase were lower or even absent.Changes in most enzyme activities were observed in the precancerous stage and the pattern of these changes followed that in the liver tumour. Thus in the course of carcinogenesis, the activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase and dipeptidase(glycylglycine as substrate)increased while those of glutamic dehydrogenase, glutaminase and ornithine carbamyl transferase decreased. However, there was no significant change in the activity of dipeptidase when DL-alanylglycine was used as substrate. Changes in activity of tryptophan pyrrolase and tyrosine transaminase were not pronounced as compared with those of the control. The activity of glutathione reductase in the liver tumour was similar to that of normal liver, but it increased from the 4th to 13th week of feeding of the carcinogen. Threonine dehydrase was remarkably influenced by the nutritive factor of the basal diet so that the effect of 3'-MeDAB on threonine dehydrase could not be observed during carcinogenesis.A comparative study has been made with 2-MeDAB, a non-carcinogenic substance. It had no apparent effect on the above enzymes except that it caused the activity of glutamic dehydrogenase to be higher than that of the control.Further experiments have shown that the specific activities of glutamic dehydrogenase and glutaminase in the mitochondria of liver tumour were lower than those of the control. In the precancerous liver the specific activity of glutaminase in the mitochondria was lower than that of the control, while there was no significant change in the case of glutamic dehydrogenase.From these results together with those from other laboratories a possible biochemical mechanism of the carcinogenesis induced by 3'-MeDAB was proposed(Fig. 12). It was suggested that the change in enzyme activity during carcinogenesis may possibly have resulted from the carcinogen being first metabolized in the liver, leading to a higher activity of the oxidative metabolism of glucose-6-phosphate and exhibiting influences on liver enzymes by the metabolites of 3'-MeDAB through different mechanisms. Consequently there produced an abnormal growth and differentiation of liver cell which became neoplastic with the formation of liver cancer, 2-MeDAB may be metabolized in a different way from that of 3'-MeDAB thus producing different effects on most enzyme activities. It is therefore evident that the specific effect of 3'-MeDAB on the liver enzymesmay be closely related to its property of carcinogenisity.

在3'-MeDAB誘发的肝癌組織中,G-6-PD、6-PGD、二肽酶的活性都較正常肝高,而另一些酶如GDH、GMA、OCT、TP、TD、TTA的活性則較正常肝低或甚至測不出来。大多数酶活性都在癌前期即有明显的变化,其变化情况多趋向于癌的特征,如肝癌組織中活性較高的酶,在引癌过程中其活性較对照組有升高趋势,如G-6-PD、6-PGD、二肽酶(以甘氨酰甘氨酸为底物);肝癌組織中活性降低的酶,在引癌过程中其活性有降低趋势,如GDH、GMA、OCT。但以丙氨酰甘氨酸为底物的二肽酶活性的变化則与对照組基本相似。癌前期TP及TTA活性較对照組都无明显差异。肝癌組織中GSSGR活性与正常肝相似,但在引癌过程中(4—13周)則有升高趋势。苏氨酸去水酶受基础食料中营养因素的影响較大,癌前期看不出3'-MeDAB对它的影响。非致癌物,2-MeDAB,除了使GDH活性升高外,对上述其他酶活性都无明显的影响。肝癌綫粒体內GMA和GDH比活性都較对照組及正常肝綫粒体为低。癌前期肝綫粒体GMA比活性較对照組显著降低,而GDH比活性則无明显改变。根据本实驗及其他实驗室結果,我們认为:3'-MeDAB所引...

在3'-MeDAB誘发的肝癌組織中,G-6-PD、6-PGD、二肽酶的活性都較正常肝高,而另一些酶如GDH、GMA、OCT、TP、TD、TTA的活性則較正常肝低或甚至測不出来。大多数酶活性都在癌前期即有明显的变化,其变化情况多趋向于癌的特征,如肝癌組織中活性較高的酶,在引癌过程中其活性較对照組有升高趋势,如G-6-PD、6-PGD、二肽酶(以甘氨酰甘氨酸为底物);肝癌組織中活性降低的酶,在引癌过程中其活性有降低趋势,如GDH、GMA、OCT。但以丙氨酰甘氨酸为底物的二肽酶活性的变化則与对照組基本相似。癌前期TP及TTA活性較对照組都无明显差异。肝癌組織中GSSGR活性与正常肝相似,但在引癌过程中(4—13周)則有升高趋势。苏氨酸去水酶受基础食料中营养因素的影响較大,癌前期看不出3'-MeDAB对它的影响。非致癌物,2-MeDAB,除了使GDH活性升高外,对上述其他酶活性都无明显的影响。肝癌綫粒体內GMA和GDH比活性都較对照組及正常肝綫粒体为低。癌前期肝綫粒体GMA比活性較对照組显著降低,而GDH比活性則无明显改变。根据本实驗及其他实驗室結果,我們认为:3'-MeDAB所引起的肝脏酶活性变化,可能是由于它在肝內进行代謝引起G-6-P旁路代謝的活跃,以及3'-MeDAB代謝产物通过各种不同机制对酶的影响所致。这些酶活性的变化可能导致肝細胞的异常生长和异常分化因而形成肝癌(图12)。非致癌物,2-MeDAB,可能与3'-MeDAB的代謝途径不同,因而产生不同的影响,而3'-MeDAB所产生的特殊影响則可能与其致癌作用有关。

 
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